This project will extend our recent studies concerning T lymphocyte responses in the lung, by evaluating the localization of T lymphocyte subpopulations, especially cytotoxic T lymphocytes (CTL) and CTL precursors. We have found that, following intraperitoneal immunization of mice with alloantigen, lung parenchyma is an enriched source of effector CTL, and is also a site where large numbers of T lymphocytes accumulate. These new T lymphocytes have unique properties, such as low density thy 1 antigen. However, the CTL are probably not derived in situ from lung, since, unlike spleen or lymph node cells, lymphocytes derived from lung parenchyma of non-immune mice cannot generate CTL during in vitro culture with antigen. We propose that stimulation by potent immunogens, by changing the properties of the lung, of recirculating cells, or both, causes localization to the lung of circulating effector CTL and other T lymphocytes. To evaluate this hypothesis, the project will define the functional deficiencies of lung cells from non-immune mice; and will evaluate the effect of in vivo antigenic stimulation on the functional composition (CTL precursors, helper T cells, etc.) of lung parenchyma. Related studies will determine whether lung T lymphocytes possess unique functional properties (e.g., NK activity). Additional experiments will compare the localization of T cell subpopulations in lungs of non-immune or antigenically stimulated mice. These studies will provide quantitative information on local, pulmonary, T lymphocyte responses.